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COPS5 activates apoptotic process. 36 / 41
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"In this study, we found that endogenous Jab1 interacts with endogenous Smad1/5/8 and p53 to modulate chondrocyte differentiation and apoptosis (Fig. 1A, C and 3C)."
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"Furthermore, the apoptosis was significantly enhanced by pJAB1."
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"Significantly, inhibition of CSN associated kinase activity or knockdown of CSN5 impairs JFK promoted p53 degradation, enhances p53 dependent transcription, and promotes cell growth suppression, G (1) arrest, and apoptosis."
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"Because cleavage of PARP and caspase-3 activation are hallmarks of the initiation of apoptosis, we further examined the influence of Jab1 on cisplatin-, IR- and UV induced apoptosis in NPC cells."
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"This implies that CSN5 intervention might concurrently induce cell apoptosis through two pathways."
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"Jab1, for example, selectively binds the marked box domain of E2F1, suggesting that Jab1 synergizes with E2F1 to promote apoptosis [45], and recent studies show that Jab1-E2F1 complexes are recruited [MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"
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"However, there were no significant differences in apoptosis induced by control and Jab1 siRNA."
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"The results of the RPPA analysis agree with our western blotting data, confirming that Jab1 depletion promotes apoptosis in NPC cells after cisplatin and UV radiation treatment."
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"Jab1 shRNA treated cells had higher levels of cleaved caspase-3 and gamma-H2AX after cisplatin, IR and UV exposure (XREF_FIG, Top), supporting our hypothesis that Jab1 depletion enhances genotoxic stress induced apoptosis and DNA damage."
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"Porcine JAB1 significantly enhances apoptosis induced by staurosporine."
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"Flow cytometric analysis proved that pJAB1 significantly enhanced apoptosis induced by staurosporine, which at least partially depended on the activation of caspase-9 and caspase-3."
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"In contrast, BclGs (Bcl-Gonad short form), a proapoptotic BH3-only protein, and Jab1 and CSN5 coexpression synergistically induced apoptosis."
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"We identified Jab1 as an E2F1 specific binding protein and showed that Jab1 and E2F1 coexpression synergistically induce apoptosis, coincident with an induction of p53 protein accumulation."
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"Jab1/CSN5 promotes E2F1-dependent induction of apoptosis as an E2F1-specific binding protein."
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"PJAB1 enhances apoptosis induced by STS."
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"Taken together, the mechanism of apoptosis enhanced by JAB1 need to be studied further."
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"By E18.5, Jab1 cKO mutant mice exhibited significantly shorter limbs with : very few hypertrophic chondrocytes, disorganized chondrocyte columns, much smaller primary ossification centers, and significantly increased apoptosis."
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"As expected, CSN5 null embryonic cells, which lacked other CSN components, expressed higher levels of p27, p53, and cyclin E, resulting in impaired proliferation and accelerated apoptosis [82] ."
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"Because cleavage of PARP is a hallmark of the apoptosis [ 18 ], we investigated the effect of Jab1 on adriamycin and cisplatin-induced apoptosis in breast cancer cells."
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"Jab1 and COPS5 promotes E2F1 dependent induction of apoptosis as an E2F1 specific binding protein."
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"CSN5 deficient mouse ES cells also displayed dysfunctional proliferation and accelerated apoptosis XREF_BIBR."
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"It is obvious that we are far from unveiling the complete mechanisms of apoptosis enhanced by pJAB1 and that further studies need to be done to answer some questions."
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"Mitochondrial damage is also an important pathway that causes apoptosis, and stigmasterol activates the mitochondrial apoptotic pathway and induces apoptosis in gallbladder cancer cells by regulating p27 and JAB1 expression [56]."
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"Sub-G1 DNA content analysis showed that JAB1 could accelerate apoptosis induced by BclGs overexpression and both BclGs and BclGs together with JAB1 induced apoptosis could be almost completely inhibit[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"
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"To explore the molecular mechanism by which JAB1 promotes BclGs-mediated apoptosis, we analyzed if JAB1 could disrupt this balance and overwhelm the effect of Bcl-2/Bcl-XL on BclGs protein."
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"As shown, GFP vector or GFP-JAB1 expression led to a slight increase of cell apoptosis (5%); GFP-BclGs expression increased the number of apoptotic cells three folds than that in case of GFP or GFP-JA[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"
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"In the presence of ectopic BclGs, knock-down of JAB1 could still inhibit BclGs-induced apoptosis ( Fig. 7 E), suggesting a critical role of JAB1 in both endogenous and exogenous BclGs-induced apoptosi[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"
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"Our study revealed that re-overexpression of CSN5 in CSN5-deleted DDP cells negated the upregulation of ATF4-CHOP pathway protein expression, mitigated apoptosis, and restored cell viability (Figure S10)."
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"Our results show that CSN5 knockdown by small interfering (si) RNA caused a strong induction of apoptosis and inhibition of cell cycle progression in HCC cells in vitro."
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"To investigate whether Jab1 deficiency enhances apoptosis, MEFs from wild-type and Jab1 +/- embryos were immunostained for phospho specific (Ser 139) histone H2AX foci (gamma-H2AX), which is known as an early indicator of the presence of DNA DSBs."
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"Importantly, JAB1 and BclGs synergistically induce apoptosis."
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"As an independent apoptotic mechanism from CSN, CSN5 can enhance apoptosis via activation of transcription factor E2F1."
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"By building on these findings, we found that Jab1 and CSN5 sensitized mouse embryonic fibroblasts to gamma radiation induced apoptosis and increased spontaneous DNA damage that could be attributed to reduced levels of the DNA repair protein Rad51 and increased levels of p53 [XREF_BIBR]."
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"Interestingly, our recent findings showed that Jab1 and CSN5 mediates resistance of NPC cell lines to apoptosis induced by cisplatin, ultraviolet (UV) radiation, and ionizing radiation (IR) [XREF_BIBR]."
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"Cops5 KO leads to decreased expression of the pluripotency marker Nanog, proliferation defect, G2/M cell-cycle arrest, and apoptosis of ESCs."
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"Interestingly, ectopic expression of JAB1 did not significantly increase apoptosis after addition of TNFalpha, presumably because it can not fully block TNFalpha mediated NF-kappaB activation (see also XREF_FIG)."
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